Coronary heart disease, hypertension, non-insulin-dependent diabetes, insulin resistance or -insensitivity and obesity are major causes of ill health in industrial societies. Disturbances of carbohydrate and lipid metabolism are a common feature of those disorders (Evans et al., 1984, J. Clin. Tnvest., 74: 1515-1525; Ferrannini et al., 1987, N. Engl. J. Med., 317: 350-357; Reaven, 1988a, Diabetes, 37: 1595-1607; Hunt et al., 1989, Arteriosclerosis, 9: 335-344; Kaplan, 1989, Arch. Intern. Med., 149: 1514-1520; McGarry, 1992, Science, 258: 766-770; Cohen et al., 1996, Science, 274: 1185-1188; Polonsky et al., 1995, N. Engl. J. Med., 334: 777-783; Reaven et al., 1996, N. Engl. J. Med., 334: 374-381). Specifically, disturbances in carbohydrate- and fatty acid metabolism associated with defects in insulin and catecholamine action are characteristic of non-insulin-dependent diabetes, metabolic Syndrome X, obesity, familial dyslipidemic hypertension and familial combined hyperlipidemia (Reaven, 1988a, supra; Reaven et al., 1988b, Diabetes, 37: 1020-1024; Martin and Jensen, 1991, J. Clin. Invest., 88: 609-613; Hunt et al., 1989, supra; Castro Cabezas et al, 1993, J. Clin. Invest., 92: 160-168; Aitman et al., 1997, Arterioscler. Thromb. Vasc. Biol., 17: 748-754; Reynisdottir et al., 1994, Diabetologia, 37: 428-435; Reynisdottir et al., 1995, J. Clin. Invest., 95: 2163-2169). These conditions are treatable by modifications of patient lifestyle (e.g., diet and exercise) and/or with medication. If the presence- or risk of developing such a condition is identified early, a therapeutic or prophylactic regimen may be begun before the well-being of the patient has been compromised, either at all or to an appreciable extent.
There is need in the art for methods of diagnosing an individual having a propensity for one or more of heart disease, hypertension, non-insulin-dependent diabetes, metabolic Syndrome X, combined hyperlipidemia and/or obesity.
It has been suggested in the art that certain parasites utilize the CD36 protein as a ligand for infection of the host cell (Oquendo et al., 1989, Cell 58:95). An example is Plasmodium falciparum, a causative agent of malaria. Thus, hosts that express a variant of CD36 protein, or fail to express CD36, may have a greater resistance to infection by such parasites. A significant fraction of individuals lacking CD36 protein have been identified in populations of Asian and African origin, whose ancestry suggests that the phenotype became commonplace due to selection pressure from frequent malarial infection. Curtis, B. R., and Aster, R. H., 1996, Transfusion 36: 331-334.
There is a need in the art for methods of determining resistance or susceptibility to infection by Plasmodium falciparum.
It has been suggested that some apparently normal individuals lack GPIV, and thus are at risk of producing antibodies against the protein when they receive blood transfusions. Curtis et al., 1996, supra; Greenwalt et al., 1992, Blood 80:1105; Yamamoto et al., 1990, Blood 76:1698.
There is a need in the art for detecting CD36 gene mutations that give rise to CD36 deficiency for purposes of tissue screening and donation.